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Biomedical subjects

V F Sagach

Publications and source records attributed to V F Sagach.

At least 55 records · Page 3Linked to original sources
PubMed1986

[The role of immune factors in the coronary, chrono- and inotropic effects of adrenomimetics].

The experiments on dogs under chloralose and urethan anesthesia have shown that intracoronary injection of anticardiac immune serum caused inversion of coronary vascular reaction to adrenaline and isoprenaline and elimination of cardiogenic depressor hemodynamic reflex, without decreasing adrenomimetic inotropic effect. The administration of immune complexes (horse serum antigens--specific rabbit antibodies) produced biphasic coronary vascular reaction to adrenaline and decreased by half reflex hypotension, without changing chrono- and inotropic adrenaline effects.

Animals↗
PubMed1985

[Effect of preliminary local myocardial hypoxia on the development of immune heart damage].

The changes in hemo- and cardiodynamics, myocardial contractility and its structural and histochemical alterations were studied in two series of experiments (immune and combined hypoxic and immune action on the myocardium) on 27 mongrel dogs anesthesized with chloralose and urethane. It was established that preliminary short-term hypoxia of the myocardium essentially increases the alterative effect of immune factors, causing a rise in the involved area as well as in the degree of metabolic shifts in this area and in the intensity of the disorders of heart function and hemodynamics.

Animals↗
PubMed1985

[Cardio- and hemodynamics of dogs in exposure of the heart to immune complexes].

The cardiovascular effects induced by in-vitro obtained immune complexes (horse serum antigens--rabbit specific antibodies) were studied in dogs. Intracoronary administration of immune complexes was followed by the development of a hypotensive reaction, with a marked decrease in the cardiac output, left ventricle performance, and impairment of pump heart function. After administering immune complexes no marked injuries to the myocardium or depression of its contractility were recorded in the acute period of the reaction. A substantial decrease of venous blood return to the heart caused by blood pooling in the venous peripheral vascular bed underlies pump heart function impairment and the decreased cardiac output.

Animals↗
PubMed1982

[Electron microscope study of the disorders of cardiomyocyte membrane permeability in immune heart lesions].

An electron microscopic tracer of colloidal lanthane was used to explore the changes occurring in cardiomyocyte sarcolemma permeability after local immune injury to the dog heart. Ion permeability of the myocyte membranes was demonstrated to be impaired rapidly (within the first 5 minutes of reaction) at the site of cardiac antibody action. The number of the cardiomyocytes with impaired sarcolemma permeability increased with time. Intracellular deposition of lanthane was accompanied by structural alterations in the cardiomyocytes: contractures, mitochondrial deformation. Pretreatment with the antihistamine drug phencarol prevented to a considerable measure the impairment of sarcolemma permeability and destruction of cardiomyocytes under immune injury to the heart.

Animals↗
PubMed1980

[Energy metabolism and myocardial contractile activity in cardiocytotoxic injury].

It was established in experiments on anesthetized dogs with a closed thorax that injection of anticardiac cytotoxix serum into one of the main branches of the left coronary artery is accompanied by regional disturbances of energy metabolism, manifested by a decrease in ATP, ADP, AMP and glycogen content, and in the contractility of a injured area of the left ventricle. Undamaged myocardium of the left and right ventricles showed a compensatory hyperfunction and an increased level of noradrenaline. The energy metabolism parameters of undamaged cardiac area do not undergo any material changes.

Animals↗
PubMed1979

[Mechanisms of blood deposition in dogs with a cytotoxic heart lesion].

The reactions of capacitance blood vessels of the abdominal cavity and pelvis were studied in vagotomized dogs during cytotoxic heart injury. The same reactions were investigated in recipient dogs during cross circulation with cardiac damage in the donors. A certain role of the neuroreflex and humoral cardiogenic factors involved in the development of increased capacity of blood vessels is shown.

Animals↗
PubMed1978

Contraction activity of right heart ventricle and pulmonary haemodynamics in cytotoxic cardiogenic shock.

In the course of experimental cardiogenic shock in dogs it was found that in comparison with marked disturbances of heart function and haemodynamics in the systemic circulation, the changes in the right ventricular contractility were less conspicuous. The pulmonary arterial pressure kept at a level approaching the initial one. The pulmonary vascular resistance substantially rose at the same time, especially so in the arterioles. The left heart filling pressure did not increase. The authors assume that the changes in the pulmonary vascular resistance result from direct neurohumoral control of vascular resistance, and discuss possible mechanism of this control.

Animals↗
PubMed1976

[Role of reactions of large-capacity blood vessels in the pathogenesis of experimental cardiogenic shock].

Reaction of the capacitance vessels of the abdominal cavity and the pelvis was studied in dogs with the cardiotoxic myocardial necrosis complicated by the cardiogenic shock. The deposit of a significant volume of the circulating blood in the venous part of the vascular reservoir of the abdominal cavity and the pelvis was observed in the course of the first minutes of acute myocardial necrosis. A substantial role of reduction of the venous return to the heart in the pathogenesis of the hemodynamic disturbances accompanying the development of the cardiogenic shock is emphasized.

Abdomen↗
PubMedDate not supplied

[Effect of sodium nitroprusside on Na+, K+-ATPase of rat myocardium and renal cortex].

The influence of NO donor, sodium nitroprusside (SNP) in concentrations of 10(-5)-10(-3) M, on the Na-pump activity in membrane preparations (microsomes) of rat miocardium and renal cortex was studied. A correlation has been observed between Na-pump activation by 31.4% and 73.6% and increase in thiol group content by 45.0% and 94.0% in native microsomes of myocardium and renal cortex by low concentrations of SNP (10(-5)-10(-4) M). The Na-pump activation as well as the increase in the number of DTNB-reactive thiol groups was abolished after the detergent treatment (0.025% sodium dodecylsulphate); however, the detergent by itself exerted similar influence on Na-pump activity and thiol group content in microsomes. A comparable effect of other oxidants (hydrogen peroxide and nitroglycerine) on SH-group content in microsomes of renal cortex was also shown. A conclusion was made that non-specific oxidative action of SNP on some membrane structures in microsome preparations led to their exposure and activation of the Na-pump by demasking of its latent activity.

Animals↗
PubMedDate not supplied

[Effect of Ca2+ on induction of the mitochondrial pore opening in the rat myocardium].

The mitochondrial role opening (MPT) induced by Ca2+ has been studied in isolated rat heart mitochondria. MPT was characterized as cyclosporine A-inhibited swelling accompanied by the loss of membrane potential (deltapsim) and Ca2+ efflux after the Ca2+ -loading which was followed spectrophotometrically after the Ca2+ -arsenaso-III complex formation. It has been shown that in suspension of isolated mitochondria MPT was activated by low (with maximum at about 20 microM Ca2+) and high concentrations of Ca2+ (the concentration curve shows a saturation at about 1.0-1.5 mM). In all the cases an access of Ca2+ ions to the matrix space of the mitochondria was necessary for MPT induction. MPT activated by low concentrations of Ca2+ was accompanied by slow decrease of deltapsim and slow release of Ca2+, enhanced by ruthenium red (RR), and was independent of the substrate used (glutamate or succinate). It had not been observed if the respiratory chain was inhibited, even if the Ca2+ access to the inner mitochondrial membrane was provided by Ca2+ -ionophore A23187. At high Ca2+ concentrations rapid Ca2+ -uptake and release via Ca2+ -uniporter (inhibited by ruthenium red) followed by extensive swelling (pore formation) have been observed. It had been supposed that rapid MPT at high concentrations of Ca2+ was the result of Ca2+ entrance to the mitochondrial matrix and depolarisation of the mitochondrial membrane. The data obtained show two different mechanisms of Ca2+ -induced MPT. The one is sensitive to the redox-state of the electron transport chain and is abolished if the respiration is inhibited. The other is independent of mitochondrial respiration and needs only Ca2+ access to the inner mitochondrial membrane and Ca2+ binding to some specific sites leading to MPT opening.

Animals↗
PubMedDate not supplied

[Decrease of mitochondrial sensitivity to Ca2+-induced pore opening during long-term incubation].

It is shown that mitochondria of rat myocardium exhibit high sensitivity to Ca2+-induced permeability transition pore (PTP) during an hour after their isolation. The threshold Ca2+ concentrations necessary to induce PTP are as low as 25-50 nmol/mg of protein. Apparent K(Ca) constant of Ca2+-dependent PTP activation is 40 microM. Incubation of mitochondria during 2, 3 and 4 hours after their isolation leads to gradual increase in K(Ca) values up to 0.4 microM, which is accompanied by simultaneous decrease in sensitivity of mitochondria to pore opening. A correlation is supposed between changes of kinetic parameters of Ca2+-uniporter and changes in sensitivity of mitochondria to Ca2+-induced permeability transition.

Animals↗
PubMedDate not supplied

[Effect of nitric oxide donors on Ca2+-uptake in the rat heart and liver mitochondria].

The influence of NO donors, nitroglycerin (NG) and sodium nitroprusside (SNP), on Ca2+- uptake in rat heart and liver mitochondria is studied. It is shown that in vivo NG causes a rapid dose-dependent increase of Ca2+-uptake in rat heart mitochondria most pronounced at 0,5-1,0 mg/kg weight NG. This sharp increase of Ca2+-uptake is not accounted for by changes in membrane potential of mitochondria (deltapsim) because deltapsim is not influenced by less than 1,0 mg/kg NG, and moreover, decrease by approximately 30% is observed at 1,0-1,5 mg/kg NG. In vitro, on the contrary, a concentration-dependent decrease in Ca2+-uptake caused by NG as well as SNP is observed together with simultaneous decrease of deltapsim and concentration-dependent release of Ca2+ from mitochondria via Ca2+-uniporter as the result of partial depolarisation of mitochondrial inner membrane. The data obtained give an evidence that increase in Ca2+-uptake caused by NO donor in vivo takes place independently of changes in deltapsim and also is not resulted from a direct action of NO on Ca2+-uniporter. These observations allow us to suppose that activation of mitochondrial Ca2+-uptake in vivo and corresponding decrease in cytosolic Ca2+ concentration could be involved in vasodilatory action of nitric oxide.

Animals↗
PubMedDate not supplied

[Calcium release from the rat liver mitochondria during collapse of the membrane potential].

Ca(2+)-release from rat liver mitochondria after protonophore (carbonyl cyanide m-chlorophenylhydrazone, CCCP)-induced membrane depolarisation is studied. It is shown that the release of calcium is accompanied by an increase of the inner mitochondrial membrane permeability as the result of the opening of permeability transition pore (PTP). Calcium is released from mitochondria through the uniporter working in reverse mode and also by PTP mechanism which accounts for ruthenium red (RR)-insensitive component of total. Ca(2+)-release. Unlike Ca2+, the strontium release from the mitochondria is completely sensitive to RR, specific uniporter blocker, which shows the absence of rapid Sr(2+)-efflux mechanisms other than uniporter of bivalent cations. The data obtained also give an evidence that the lifetime of the open state of the pore is limited, and barrier properties of the mitochondrial membrane are restored after the closure of the pore.

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